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Presenilin-1 controls glucose metabolism and identity of pancreatic beta cells

Koshenov, Z.; Postic, S.; Schosiwohl, G.; van Amsterdam, S.; Hois-Zelinka, V.; Oflaz, F. E.; Rost, R.; Tiapko, O.; Gottschalk, B.; Hirtl, M.; Bachkoenig, O. G.; Koshenova, A.; Erdogan, Y. C.; Sagintayev, A.; Krnjic, A.; Pfabe, J.; Sarikas, S.; Hochreiter, B.; Gindlhuber, J.; Schittmayer, M.; Tadic, J.; Ehall, B.; Madeo, F.; Madl, T.; Malli, R.; Birner-Gruenberger, R.; Pieber, T.; Eisenberg, T.; Slak Rupnik, M.; Graier, W. F.

2025-09-05 cell biology
10.1101/2025.09.05.674426 bioRxiv
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AbstractPresenilin 1 is an endoplasmic reticulum protein, most known for its role in pathogenesis of familial Alzheimers Disease (AD). Presenilin 1 has been attributed roles in intracellular calcium homeostasis in the brain, as well as in the pancreatic beta cells, where it has been shown to be fundamental for glucose-induced insulin secretion. Functional similarity of presenilin 1 in regulation of intracellular calcium homeostasis in the brain and pancreas prompted us to investigate a prevalent assumption that associates AD and diabetes mellitus. By examining pancreatic islets from AD model mice, we have found deficits in initial phase of glucose-induced calcium signaling and insulin secretion. Furthermore, these transgenic mice showed a tendency towards reduced expression of mature beta cell markers, which was even more pronounced in islets and beta cell lines with a transient knock down of presenilin 1. We demonstrate here that presenilin 1 controls beta cell glycolysis by regulating sub-cellular calcium homeostasis and, in doing so, contributes to preservation of beta cell identity.

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